The investigators hypothesize that following shock from either hemorrhage or thermal injury; there is a release of mediators from the gastrointestinal tract, which interact with mesenteric lymphatic system to cause the release of cytotoxic mediators from the mesenteric lymph nodes. The materials from the lymph nodes activate of pulmonary endothelium resulting in the adherence of leukocytes to the pulmonary microvasculature, and pulmonary vascular injury. In their first specific aim the investigators will characterize the action of shock lymph on endothelial cells and neutrophils and identify the humoral factors present in the mesenteric lymph after injury. The second specific aim they will determine the role of adherence molecule expression on the shock induced lung injury. The final specific aim will determine mechanisms by which mesenteric lymph from blood or burned rats, produces the lung injury. They will determine how diversion of the lymphatic drainage from the gut will prevent the pulmonary changes (deposition of cells in the lung, expression of adherence molecules and cytokines) associated with hypovolemic and burn shock. They will inject lymph into the animals and evaluate changes in the lung. This work will help to determine why disruption of gut barrier function will lead to lung injury. It will also more clearly define the role of the gut inducing lung injury and in the development of the systemic inflammatory response syndrome and multiple organ failure (MOF).